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Mice lacking a functional CHK gene have no apparent defects in the hematopoietic system
Author(s) -
Samokhvalov Igor,
Hendrikx Jan,
Visser Jan,
Belyavsky Alexander,
Sotiropolous Damianos,
Gu Hua
Publication year - 1997
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549700203881
Subject(s) - haematopoiesis , mutant , biology , in vivo , tyrosine kinase , mutation , gene , ex vivo , receptor tyrosine kinase , microbiology and biotechnology , signal transduction , stem cell , genetics
Non‐receptor tyrosine kinase Chk has been implicated in hematopoietic development. To study the function of Chk in vivo, we have generated chk‐deficient mice using gene targeting. Overall development of mice homozygous for this mutation was apparently normal. Blood counts, FACS analysis of hematopoietic cell populations, CFU‐C and CAFC assays showed no significant difference between wild type and mutant animals. Thus, the dispensability of Chk for mouse development and hematopoiesis suggests that its function may be redundant in vivo, and most likely be compensated by activity of a closely related protein tyrosine kinase Csk.